Proposed Model of the SynGAP-Mediated Cellular Signaling Pathway that Regulates Translation and Synaptic AMPAR Content.

<p>Our data predict the following model: under conditions of basal neuronal activity, association of GluN2B and CaMKII links SynGAP to suppression of ERK signaling. ERK can activate Rheb, which, in turn, activates mTOR. Through suppression of mTOR function this mechanism inhibits protein synthesis and limits AMPAR contribution at developing cortical networks. Our data show that this signaling pathway is critical for developmental synaptic plasticity as translation-dependent homeostatic synaptic plasticity is disrupted in the absence of GluN2B or SynGAP.